Carotid Artery-Related Perioperative Stroke Following Anterior Cervical Spine Surgery: A Series of 3 Cases and Literature Review

Background

Vascular complications following anterior cervical spine surgery are rare but potentially devastating. Complications associated with the carotid artery are even more disastrous but largely anecdotal, with no more than 4 reported cases.

微RNA-210抑制人退行性变髓核细胞自噬影响椎间盘退行性变

目的探讨微RNA-210(miRNA-210)对退行性变髓核细胞自噬的影响及其参与椎间盘退行性变(IDD)进程的可能机制。方法收集24例IDD患者(IDD组)和6例腰椎骨折患者(对照组)椎间盘组织进行分离,培养髓核细胞。通过实时荧光定量聚合酶链反应(FQ-PCR)检测髓核细胞中miRNA-210的表达,通过单丹磺酰尸胺(MDC)染色和蛋白质印迹法检测细胞自噬水平。通过FQ-PCR或蛋白质印迹法检测过表达或抑制miRNA-210对细胞自噬和细胞外基质代谢的影响。通过生物信息学手段寻找miRNA-210与自噬相关的靶基因及miRNA-210的结合位点,并应用双荧光素酶报告实验验证。结果与对照组相比,IDD组髓核细胞中miRNA-210表达量增加,细胞自噬水平降低。过表达miRNA-210会抑制髓核细胞自噬,同时降低Ⅱ型胶原(ColⅡ)及蛋白多糖表达量,升高基质金属蛋白酶-3(MMP-3)和MMP-13表达量。自噬抑制剂3-MA减弱miRNA-210对ColⅡ、蛋白多糖、MMP-3和MMP-13的调节作用。miRNA-210与自噬相关蛋白7(ATG7)存在结合位点,过表达miRNA-210通过沉默ATG7抑制细胞自噬,激活MMP-3和MMP-13,促进细胞外基质(ColⅡ和蛋白多糖)降解。结论在发生退行性变的椎间盘组织中miRNA-210表达量增加。过表达的miRNA-210可能通过直接作用于靶基因ATG7抑制细胞自噬,促进细胞外基质降解,推动IDD进程。     

Comparison of anterior cervical discectomy and fusion with the zero-profile device versus plate and cage in treating cervical degenerative disc disease: A meta-analysis

Zero-profile device was applied to diminish the irritation of the esophagus in the treatment of cervical degenerative disc disease. However, the clinical application of the zero-profile device has not been testified with clinical evidence. The aim of the meta-analysis was to systematically compare the safety and effectiveness of anterior cervical discectomy and fusion with zero-profile device with plate and cage for the treatment of cervical degenerative disc disease. Electronic searches of PubMed and Embase were conducted up to May 2015. Relevant studies were included. Weighted mean difference (WMD) and 95% confidence intervals (CI) were assessed for continuous data. Risk ratio (RR) and 95% CI were assessed for dichotomous data. P value <0.05 was considered to be significant. Eleven studies were included in the meta-analysis. Compared with plate and cage, zero-p is associated with lower operation time of two-level surgery, less intraoperative blood loss, higher subsidence rate, higher JOA score, lower incidence of dysphagia in short-term (RR: 0.72, 95% CI [0.58, 0.90], P = 0.005, I² = 22%) and long-term (RR: 0.12, 95% CI [0.05, 0.30], P < 0.00001, I² = 0%) and lower Cobb angle of multilevel surgery (WMD: −3.16, 95% CI: [−4.35, −1.97], P < 0.00001, I² = 0%). No significant difference was found in one-level and two-level Cobb angle, fusion rate and operation time of one-level and three-level surgery. Both zero-p implantation and the plate and cage have respective advantages and disadvantages.     

Comparison Between Oblique Pulling Spinal Manipulation and Other Treatments for Lumbar Disc Herniation: A Systematic Review and Meta-Analysis

Objective

The purpose of this review was to compare oblique pulling spinal manipulation with other treatments for lumbar disc herniation.

Piezo1 activates the NLRP3 inflammasome in nucleus pulposus cell-mediated by Ca2+/NF-κB pathway

Studying and understanding the mechanism of inflammation in nucleus pulposus is the key to understand and prevent intervertebral disc degeneration. We propose a model of mechanical sensitive ion channel Piezo1 mediated inflammation of nucleus pulposus cells. Piezo1 can up-regulate the level of interleukin-1β (IL-1β) in nucleus pulposus cells once it is activated. It is suggested that Piezo1 may mediate inflammation by activating Nod-like receptor protein 3 (NLRP3) inflammasome to accelerate the production and maturation of IL-1β. The primary objective of this study was to explore whether Piezo1 activates NLRP3 inflammasome in nucleus pulposus cells. Piezo1 sensitization was induced by mechanical stretch following which we analyzed the priming and assembly of NLRP3 inflammasome and also studied if the downstream Ca²⁺/NF-κB pathway mediated this activation in nucleus pulposus cells. The expression of Piezo1 and NLRP3 inflammasome increased in a time-dependent manner upon mechanical stretch. Piezo1 activation promoted NLRP3 inflammasome assembly, which was demonstrated by the upregulation of caspase-1 activation and IL-1β production. Transfection of Piezo1-siRNA reversed this process. The inhibition of Ca²⁺/NF-κB pathway reduced Piezo1-dependent activation of NLRP3 inflammasome. Thus, we propose that activation of NLRP3 inflammasome in nucleus pulposus cells mediated by Piezo1 through the Ca²⁺/NF-κB pathway is a novel pathogenesis for the progress of intervertebral disc degeneration. As per our knowledge this is the first study which has provided evidence linking Piezo1-mediated inflammation in nucleus pulposus cells with the production of NLRP3 inflammasome.     

Upregulation of Sirt1 by tyrosol suppresses apoptosis and inflammation and modulates extracellular matrix remodeling in interleukin-1β-stimulated human nucleus pulposus cells through activation of PI3K/Akt pathway

Intervertebral disc degeneration (IDD) is the major pathogenesis of lower back pain. Tyrosol is a polyphenolic compound that exhibits anti-oxidant, anti-apoptotic, and anti-inflammatory effects. Herein, we explored the effects and mechanisms of tyrosol on IDD progression in interleukin (IL)-1β-stimulated human nucleus pulposus cells (HNPCs). Cell viability and apoptosis were detected by CCK-8 and flow cytometry analysis, respectively. The production of tumor necrosis factor-α (TNF-α), IL-6, nitric oxide (NO), and prostaglandin E2 (PGE2) was examined to evaluate inflammation. The mRNA expression of matrix metalloproteinases (MMPs) (MMP-3/9/13), collagen type II, SRY-related high mobility group box 9 (SOX-9), and aggrecan was measured by qRT-PCR. Protein levels of silent information regulator 2 homolog 1 (Sirt1), phosphorylated protein kinase B (p-Akt), Akt, collagen type II, SOX-9, and aggrecan were determined by western blot. Results showed that tyrosol attenuated IL-1β-induced viability reduction, apoptosis, and caspase-3/7 activity in HNPCs. The increase in the production of TNF-α, IL-6, NO, and PGE2 in IL-1β-treated HNPCs was abolished by tyrosol treatment. Tyrosol treatment reversed IL-1β-induced upregulation of MMP-3, MMP-9, and MMP-13, and downregulation of collagen II, SOX-9, and aggrecan in HNPCs. Additionally, tyrosol treatment activated the phosphatidylinositol 3-kinase (PI3K)/Akt pathway in IL-1β-stimulated HNPCs. Sirt1 was upregulated by tyrosol, and Sirt1 silencing inhibited Akt phosphorylation in HNPCs. Sirt1 knockdown attenuated the effects of tyrosol on IL-1β-induced apoptosis, inflammation, and ECM remodeling in HNPCs. In summary, upregulation of Sirt1 by tyrosol suppressed apoptosis and inflammation and regulated ECM remodeling in IL-1β-stimulated HNPCs through activation of PI3K/Akt pathway.     

Growth Factors in Intervertebral Disc Homeostasis

Intervertebral disc degeneration is a complex age-related pathology associated with back pain. Research on the growth factors that regulate disc homeostasis is of critical importance for understanding the basis of the disease. Here we summarize the data on the expression and function of various growth factors in the disc from in vivo and in vitro studies, as well as on their alterations during degeneration and ageing. Such studies are becoming more crucial in the prospect of clinical application of growth factors for the treatment of disc degeneration.     

Effects of degenerated intervertebral discs on intersegmental rotations,intradiscal pressures,and facet joint forces of the whole lumbar spine

The effects of intervertebral disc (IVD) degeneration on biomechanics of the lumbar spine were analyzed. Finite element models of the lumbar spine with various degrees of IVD degeneration at the L4-L5 functional spinal unit (FSU) were developed and validated. With progression of degeneration, intersegmental rotation at the degenerated FSU decreased in flexion–extension and left–right lateral bending, intradiscal pressure at the adjacent FSUs increased in flexion and lateral bending, and facet joint forces at the degenerated FSU increased in lateral bending and axial rotation. These results could provide fundamental information for understanding the mechanism of injuries caused by IVD degeneration.     

能谱CT在钛笼椎间植骨融合评估中的应用研究

目的:探讨能谱CT在钛笼椎间植骨融合评估中的应用价值。方法:对28例脊柱钛笼椎间植骨融合术后患者行能谱CT扫描,扫描后获得常规混合能量图像(Mixed)及110 keV单能图像(GSI)。在工作站测量Mixed图像及GSI图像的噪声(SD)及信噪比(SNR)。由两位不同年资放射科医师使用5分法分别对同一患者的Mixed和GSI图像的伪影大小及植骨显示的清晰度进行评分,并分别根据Brantigan-Steffee-Fraser(BSF)分级法对钛笼内植骨融合情况进行分级。结果:两位评分者的评分一致性较好(ICC>0.60)。相对于Mixed图像,GSI图像噪声减低(t=15.292,P<0.001),SNR增加(t=-7.749,P<0.001)。每一位评分者对GSI图像与Mixed图像的伪影评分之间、植骨清晰程度评分之间差异均具有统计学意义(P均<0.001)。虽然GSI图像与Mixed图像的BSF分级差异没有统计学意义(Reader 1:Z=-1.633,P=0.102>0.05;Reader2:Z=-1.342,P=0.180>0.05),但有两位患者的BSF评分在使用GSI图像后发生了变化。结论:GSI可有效减少噪声及金属伪影,提高图像质量,使得钛笼内植骨显示更清晰,有利于评估钛笼内椎间植骨融合情况。     

Inflamación en la hernia del disco intervertebral

Up until fairly recently, it was thought that sciatic pain in the lumbar herniated disc was caused by compression on the nerve root. However, the lumbar herniated disc shows mixed pictures which are difficult to explain by simple mechanical compromise. In recent years various immunology, immunohistochemistry and molecular biology studies have shown that the herniated tissue is not an inert material, but rather it Is biologically very active with the capability of expressing a series of inflammatory mediators: cytokines such as interleukin-1, interleukin-6, interleuquin-8 and tumor necrosis factor being the ones which stand out. The inflammation is not only induced by the chemical irritation of the bioactive substances released by the nucleus pulposus but also by an autoimmune response against itself. Thus, in addition to the mechanical factor, the biomechanical mediation plays an important role in the pathophysiology of sciatic pain and of radiculopathy. Through a review of a wide range of literature, we researched the cellular molecular mediators involved in this inflammatory process around the lumbar herniated disc and its involvement in sciatic pain.